Review Article

Diagnostic and Therapeutic Strategies for Peritoneal

Tuberculosis: A Review
David C. Wu, Leon D. Averbukh* and George Y. Wu
Department of Medicine, Division of Gastroenterology-Hepatology, University of Connecticut Health Center, Farmington, CT, USA

Abstract
Peritoneal tuberculosis (PTB), although rarer than its pulmo-
nary counterpart, is a serious health concern in regions of the
world with high tuberculosis prevalence. Individuals with
baseline immunocompromise condition, whether acquired or
medically induced, are at greatest risk for experiencing PTB.
While medical treatment of the condition is similar to that of
the pulmonary disease, the generally immunocompromised
state of those infected with PTB, along with a lack of highly
sensitive and specific testing methods make early diagnosis
difficult. This review discusses the risks factors, clinical
features, diagnostic methods, and treatment options for PTB.
Citation of this article: Wu DC, Averbukh LD, Wu GY. Diag-
nostic and therapeutic strategies for peritoneal tuberculosis:
A review. J Clin Transl Hepatol 2019;7(2):140–148. doi:
10.14218/JCTH.2018.00062.
Introduction
Tuberculosis (TB) therapy and the generally improving socio-
economic status worldwide have decreased the burden of TB.
However, one-fourth of the world’s population continues to be
infected with TB.1 Regions of southeast Asia, the Western
Pacific and sub-Saharan Africa remain particularly affected.
While most cases of TB are pulmonary, the rate of abdominal
cavity infection and its contents, identified as abdominal TB,
appears to be rising and is currently the 6th most common
extrapulmonary site for TB infection.2 TB of the peritoneum
(PTB) accounts for about 25–50% of abdominal TB cases and
0.1–0.7% of all TB cases.3
The rising prevalence of abdominal TB, and along with it
PTB, is thought to be secondary to the increasing prevalence
with equal rates amongst both sexes and has a strong corre-
lation with lower socioeconomic status, poor hygiene, and
overcrowding.6 In this review, we discuss the clinical fea-
tures, pathogenesis, diagnostic techniques, and therapy for
PTB, a specific subtype of abdominal TB affecting the
peritoneum.
Clinical features
PTB is difficult to diagnose clinically, given its nonspecific
features that often overlap with many other chronic conditions,
such as liver cirrhosis and autoimmune deficiency syndrome
(commonly known as AIDS). Classically, PTB presents as one
of three different variants: wet-ascitic, fibrotic-fixed, and dry
plastic.7 The wet-ascitic type is defined by large amounts of
loculated or high protein ascitic fluid. The fibrotic type is char-
acterized by interloped adhesions of bowel along the omentum
and mesentery. The dry plastic type is characterized by a gross
inflammatory reaction demonstrated by diffuse fibrous adhe-
sions and nodules all along the peritoneum. It should be noted,
however, that PTB can present as a combination of these three
variants.
On presentation, there is significant variability in symptom
onset and duration, ranging from several weeks to months.
Most commonly, patients present with signs and symptoms of
vague abdominal pain, weight loss, fever, abdominal ascites,
abdominal distension, abdominal mass, and abdominal ten-
derness7–12 (Table 1).
Table 1. Literature8,10,11,37,39,44,75–85 review of commonly described
symptoms and signs of PTB

of immunocompromised states, including human immunode- Characterization Total/ Avg frequency

ficiency virus (HIV) infection and alcoholic liver disease, as
well as of increased migration into endemic regions.4,5 PTB Number of cases 1725
most commonly affects those between the ages of 35–45 Symptoms

Keywords: Peritoneal tuberculosis; Tuberculosis; Liver disease; Human

Abdominal pain 75.0%
immunodeficiency virus. Weight loss 53.0%
Abbreviations: ADA, adenosine deaminase; AIDS, autoimmune deficiency syn-
drome; HIV, human immunodeficiency virus; IGRA, interferon gamma release Signs
assay; INH, isoniazid; MCP-1, monocyte chemoattractant protein-1; PTB, perito-
Fever 69.0%
neal tuberculosis; QFT-GIT, quantiferon gold-TB gold in-tube; RIF, rifampin; SAAG,
serum-ascites albumin gradient; TB, tuberculosis; TNFa, tumor necrosis factor ascites 62.0%
alpha; TLR, Toll-like receptor.
Received: 12 December 2018; Revised: 8 March 2019; Accepted: 14 March 2019 Abdominal distension 60.0%
*Correspondence to: Leon D. Averbukh, Department of Medicine, Division of
Abdominal mass 34.0%
Gastroenterology-Hepatology, University of Connecticut Health Center, 236 Farm-
ington Ave., Farmington, CT 06030, USA. Tel: +1-347-306-4752, Fax: +1-860- Abdominal tenderness 49.0%
679-4613, E-mail: averbukh@uchc.edu

140 Journal of Clinical and Translational Hepatology 2019 vol. 7 | 140–148

Copyright: © 2019 Authors. This article has been published under the terms of Creative Commons Attribution-NonCommercial 4.0 International (CC BY-NC 4.0), which
permits noncommercial unrestricted use, distribution, and reproduction in any medium, provided that the following statement is provided. “This article has been published
in Journal of Clinical and Translational Hepatology at DOI: 10.14218/JCTH.2018.00062 and can also be viewed on the Journal’s website at http://www.jcthnet.com”.
Wu D.C. et al: Peritoneal tuberculosis: A review

Susceptibility and mechanisms of pathogenesis
Most commonly, PTB develops as a result of reactivation of
latent TB. The pathologic mechanism involves the activation
of localized tuberculous focus in the peritoneum created by
the hematogenous spread of bacteria from the primary
pulmonary focus by mesenteric lymph nodes during prior
infection. PTB can less commonly develop in the setting of
active pulmonary of miliary TB by the same mechanism13
(Figs. 1 and 2). Alternative routes of infection include inges-
tion of bacilli with subsequent passage to mesenteric lymph
nodes through the Peyer’s patches in intestinal mucosa as
well as contiguous spread from infected lymph nodes, ileoce-
cal TB, or genitourinary TB.14 Although very rare, PTB caused
by Mycobacterium bovis rather than M. tuberculosis has been
noted to occur following the ingestion of unpasteurized
milk.15
Infectious disease: HIV
HIV is one of the most significant risk factors for the develop-
ment of both pulmonary and extrapulmonary TB. Up to 50%
of patients with active TB who are HIV positive develop
extrapulmonary manifestations, as compared to only 10–
15% of those who have active TB but are HIV negative.16
Clinically important is the finding that PTB in patients with
untreated HIV may be relatively asymptomatic and can go
undiagnosed due to the patient’s inability to mount an
immune response. In one case report, a patient’s PTB was
diagnosed only after experiencing immune reconstitution
syndrome following initiation of antiretroviral therapy for
HIV.17 The mechanism behind the increased susceptibility
for PTB in HIV patients lies in the impairment of the T-helper
cell 1-type immune response, a crucial part of the adaptive
immune system for TB defense.18
Immunomodulating medications
Immunomodulating medications have been implicated as
significant risk factors for PTB. Patients on tumor necrosis
factor alpha (TNFa) inhibitor therapy for autoimmune disor-
ders, including Crohn’s disease and psoriasis, have been
noted to be at risk for TB reactivation.19–21 The mechanism
behind this reactivation is believed to be due to the role TNFa
plays in inducing granuloma formation, thereby controlling
bacterial growth and limiting bacterial dissemination and
tissue damage during TB infection. With TNFa blocking
medications such as infliximab and adalimumab, granuloma
formation and maintenance is impaired and the likelihood of
disseminated disease increases.19–23 Other inflammatory
modulating medications, such as corticosteroids, have also
been shown to increase the risk of developing PTB.15
Pathologic states: Liver cirrhosis, diabetes mellitus,
and renal failure requiring dialysis
Liver cirrhosis, diabetes mellitus, and renal failure requiring
continuous ambulatory peritoneal dialysis have all been
demonstrated to be significant risk factors in the development
of PTB.24–26 Cirrhotic patients have significantly higher rates
of pulmonary TB infection. In one study, the infection rate in
cirrhotic patients was found to be nearly 15 times that of the
general population.24 Additionally, cirrhotic patients are sig-
nificantly more likely to exhibit extrapulmonary TB (31% vs.

Fig. 1. Mechanisms of PTB development. There are three main pathways through which TB infects the peritoneum. In most cases, the bacterial spread is achieved by
reactivation of TB in the lungs (or other solid organs) and subsequent hematogenous or lymphatic spread to the peritoneum (depicted in 1). Though rare, peritoneal infection
by the intestinal tract is possible due to the ingestion of infected milk or sputum. In this pathway, the TB infects the mucosal layer of the gastrointestinal tract, with sub-
sequent formation of epithelioid tubercles in the lymphoid tissue of the submucosa. Caseous necrosis of the tubercles in roughly 2–4 weeks leads to mucosal ulceration and
can lead to infection of deeper layers of the intestines and eventually into adjacent lymph nodes and peritoneum (depicted in 2). The third pathway of peritoneal infection
involves the direct spread to the peritoneum from an infected adjacent focus, such as the fallopian tubes (pictured) or a psoas abscess74 (depicted in 3). The icons were
adapted from flaticon.com. Abbreviations: PTB, peritoneal tuberculosis; TB, tuberculosis.

Journal of Clinical and Translational Hepatology 2019 vol. 7 | 140–148 141

 Wu D.C. et al: Peritoneal tuberculosis: A review

Fig. 2. Formation of the TB granuloma in primary lung infection and subsequent spread. Following the inhalation of contaminated aerosols, Mycobacterium
tuberculosis is recognized by macrophages in the lung alveoli by surface receptors (depicted in 1). Subsequently, the bacteria are taken up by macrophages which, along with
epithelial cells and neutrophils, trigger innate immune signaling pathways that allow for the production of chemokines and cytokines (depicted in 2). The release of
chemokines and cytokines recruits more macrophages, lymphocytes, and dendritic cells to the infection site, where they form granulomas composed of infected macro-
phages in the middle, surrounded by lymphocytes (CD4+, CD8+, gamma/delta T cells). The conglomerated macrophages can also fuse to form multinucleated giant cells or
differentiate into lipid rich foamy cells (depicted in 3 and 4). Within the granuloma, bacteria can survive for years, in a latent disease state. However, once triggered by
external factors, such as additional immunocompromising states, the bacteria can reactivate, killing the core infected macrophages and, thereby, producing a necrotic zone
at the center of the granuloma known as a caseum (depicted in 4). The granulomatous structure weakens with the caseum and eventually breaks down, releasing bacteria
through the body by blood, lymph, and infectious aerosolized droplets. Abbreviation: TB, tuberculosis.

12% in the general population) with the predominant mani-
festation being peritoneal.27 The etiology of cirrhosis also
appears to be important as alcohol abuse and was found to
be an underlying cause in up to as many as 90% of cirrhotic
patients with PTB.28 The mechanism behind the increased risk
of PTB in cirrhosis secondary to alcoholic liver disease is
unknown, though it has been hypothesized to involve the
cumulative effects of factors not as prominent in nonalcoholic
liver disease cases of cirrhosis, such as malnutrition and
impaired T cell-dependent function.2
Diabetes has been identified as a significant risk factor for
PTB susceptibility. In one Taiwanese study, the incidence of
PTB in diabetics was as high as 26.7%, as opposed to 6.7% in
nondiabetics.29 The reason for an increased risk of PTB in
diabetics is believed to involve reduced phagocytic capability
of peritoneal macrophages.30 Studies involving a murine
model showed that among those infected with TB, diabetic
mice, when compared to their non-diabetic peers, had signifi-
cantly higher bacillary loads in the abdominal cavity. The iso-
lated macrophages of the diabetic mice showed lower uptake
of mycolic acid-coated beads, reduced bacterial internaliza-
tion and killing, and altered cytokine responses by TNFa,
monocyte chemoattractant protein-1 (commonly known as
MCP-1) and interleukin-6 (commonly known as IL-6). The
diabetic mice also displayed more inflammatory lesions than
their nondiabetic counterparts.30
Patients with end-stage renal failure on continuous ambu-
latory peritoneal dialysis have been found to be at signifi-
cantly higher risk for PTB, when compared to the general
population, especially in developing countries and south
Asia.31 Patients with renal failure are at higher risk for PTB
secondary to their deficiency in cell-mediated immunity.32
Additionally, the dialysis effluent used in continuous ambula-
tory peritoneal dialysis is bioincompatible due to its increased
glucose concentration and nonphysiologic pH, impairing
phagocytic and lymphocytic activity in the peritoneum and
increasing risk of disseminated infection.32
Genetic variables
Recent studies have found that Toll-like receptors, such as
TLR-2, that play a key role in the innate immune system are
important in host defense against M. tuberculosis.33 Polymor-
phisms of TLR-2 have been shown to significantly impact sus-
ceptibility or resistance to TB.34 Though these polymorphisms
have generally been studied in pulmonary TB, one series

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Wu D.C. et al: Peritoneal tuberculosis: A review
investigated cases of PTB and found that there was a signifi-
cant association between the GA genotype (heterozygous
mutant) of TLR-2 Arg753Gln polymorphism and the risk of
infection with PTB.33 This suggests that individuals with
genetic polymorphisms of the Arg753Gln portion of TLR-2
may be at increased risk of developing PTB, as compared to
those with nonmutant variants. Currently, however, there is
no support for polymorphism screening in patients.
Diagnostic methods for PTB
Hematological tests
PTB is insidious and difficult to diagnose. Routine hematologic
tests are nonspecific, as the most frequent hematologic
findings include moderate normochromic normocytic
anemia, thrombocytosis, and white blood cell counts within
normal limits.14
Interferon gamma release assays (IGRAs), such as quan-
tiferon gold-TB gold in-tube (QFT-GIT) and T-spot TB, are in
vitro assays that quantify the level of interferon gamma
released by T-lymphocytes in a blood sample after exposure
to synthetic TB antigen (e.g., ESAT-6) which are normally
absent from the bacillus Calmette–Guérin vaccine. These
assays are dependent on primary versus secondary immuno-
logic response, in which the second response lymphocytes
produce a larger amount of interferon gamma relative to the
primary response. Therefore, these tests demonstrate a
patient’s exposure to TB but are unable to distinguish
between latent and active infections. Unfortunately, due to
the molecular mechanism behind IGRA testing, the frequently
immunocompromised states of those with PTB will likely
result in reduced test sensitivities/ indeterminate results.
For these reasons, IGRAs alone are insufficient in diagnos-
ing PTB. In one meta-analysis on extrapulmonary TB, in a
total of 1,711 patients in low- and middle-income countries,
the pooled sensitivity for QFT-G was only 72% [95% CI: 56–
79%] and 90% [95% CI: 86%–93%] for T-SPOT.35 However,
if used in conjunction with radiologic and clinical assess-
ments, IGRAs may help increase diagnostic power in those
with suspected PTB.36
Ascitic fluid tests
Ascitic fluid analysis is frequently performed for patients with
suspected PTB. The most common ascitic fluid tests include
acid-fast bacilli stain/smear and culture, white blood cell
count, lactate dehydrogenase, serum-ascites albumin gra-
dient (SAAG) score, and cancer antigen-125. Acid-fast bacilli
staining and Ziehl-Neelsen staining of aspirated ascitic fluid
are generally insensitive up to 3%, while bacterial culture
sensitivities range from 21–35%.37,38 In patients with PTB
and ascites, ascitic aspirate for white blood cell count varies
widely depending on the patient immune status, from as low
as 500 to as high as 1500 cells/mm3. The exception to this
finding are patients with renal failure, in whom the predom-
inant ascitic fluid cell type has been reported to be neutro-
philic.2,12,39 At this time, the discrepancy in cell types
between those with renal failure and those without is not
well understood.
Within the last 10 years, the role of IGRAs in the diagnosis
of PTB in ascitic fluid has gained momentum. In a 2015 meta-
analysis, investigators found that the diagnostic accuracy of
QFT-GIT with T-SPOT TB was greater in IGRAs of extra-
Journal of Clinical and Translational Hepatology 2019 vol. 7 | 140–148
sanguineous body fluid compared with peripheral blood.
This is most likely due to the higher concentration of lympho-
cytes within the body compartments that have the highest TB
load. Additionally, these studies found that the T-spot TB test
outperformed QFT-GIT in both sensitivity, 95% with 95% CI:
92–96, and specificity, 78% with 95% CI: 69–85).40
However, application of this information for diagnosis of PTB
is limited as the sample size of analyzed peritoneal fluid was
small compared with extra-pulmonary fluid sources.
Biochemical tests
Of the biochemical tests conducted on PTB ascitic fluid,
lactate dehydrogenase has the highest pooled sensitivity,
averaging around 77%. However, lactate dehydrogenase
provides a similar sensitivity for other diseases, such as
pancreatic ascites and peritoneal carcinomatosis, and there-
fore does not provide discriminatory value without clinical
correlation.41
When evaluating ascitic protein levels, a SAAG can be
calculated to help differentiate ascites secondary to portal
hypertension from nonportal sources. The SAAG is calculated
by subtracting the ascitic albumin level from the serum
albumin level. A SAAG <1.1 g/L can have up to 100%
sensitivity for ascites of nonportal etiology in patients with
PTB and no complicating chronic liver disease.42,43 In cases
where PTB diagnosis is complicated by chronic liver disease,
the sensitivity of this calculation drops significantly to 28–
88%.41,42 Unfortunately, in both cases, the specificity of the
test remains poor.
Cancer antigen (commonly known as CA)-125 is a sensi-
tive, but nonspecific tumor marker for ovarian carcinoma that
has been reported to be increased in PTB. At cutoffs of 35 U/
mL, CA-125 was found to have an average sensitivity of
83.33% and a specificity of 50% for PTB. The degree of CA-
125 increase may be useful in diagnostically differentiating
PTB and ovarian carcinoma, although little data exists on the
subject at this time.2,43,44
Adenosine deaminase (ADA) levels and PCR are newer
ascitic molecular diagnostic tools to detect mycobacteria.
ADA, an aminohydrolase involved in purine metabolism, is a
potent modulator of T cell differentiation.45 Recent studies
examining ADA as a molecular marker for PTB found a propor-
tional increase in differentiation of T cells in response to TB
antigen. Test sensitivities and specificities were noted to be
>90% with ascitic ADA levels >30 U/L.2,8,12,39–48
Gene amplification techniques, like real-time PCR, have
also shown tremendous potential. The Xpert nested real-time
MTB/ rifampin (RIF) PCR (CepheidGeneXpert! System, USA),
approved for use by the World Health Organization in 2010,
has demonstrated initial sensitivities and specificities as high
as 93.7% and 91.7%, respectively, in cases of pulmonary
TB.49 In a recent meta-analysis of 4461 samples comparing
Xpert MTB/RIF assay with culture or composite standard, the
Xpert pooled sensitivity and specificity was demonstrated to
be 83.1% [95% CI: 71.4–90.7%] and 81.2% [95% CI: 72.4–
87.7%], respectively.50 One study looking at the diagnostic
accuracy of Xpert MTB in 16,213 specimens presumed to
have EPTB found the pooled Xpert sensitivity to range from
31% in pleural tissue to 97% in bone or joint, while the pooled
Xpert specificity ranged from 99% in pleural tissues to 82% in
bone or joint.51 The majority of studies support Xpert MTB as
an excellent diagnostic test for ruling in EPTB, especially when
there is a positive confirmed culture. Unfortunately, it appears
143

Fig. 3. Proposed algorithm for diagnostic strategies in PTB, adapted and modified from Sinai, 2005. Abbreviation: PTB, peritoneal tuberculosis.
that Xpert MTB may have significant variability in sensitivity
relative to the tissue being sampled.50,51
Additional studies attempting to improve on the headway
made in gene amplification include studies on multiplex PCR
with selected gene targets previously determined to have
high specificity for TB such as mycobacterial protein 64 and
insertion sequence 6110. In addition to increasing the general
sensitivity of the assay, these new targets also have the
added benefit of bypassing the high cost of the Xpert assay. In
one study comparing the Xpert MTB/RIF assay with multiplex
PCR in the detection of TB in suspected pulmonary TB,
multiplex PCR had a higher sensitivity and specificity (sensi-
tivity of 100.0% and specificity of 66.7%) than Xpert MTB/RIF
(sensitivity of 78.6% and specificity of 33.3%).52 A number of
other studies looking at multiplex PCR in the diagnosis of
extrapulmonary TB suggested a pooled sensitivity of
roughly 94.5%.53–56 It should be noted that gene amplifica-
tion techniques are only as good as the sequence of probes
144 Journal of Clinical and Translational Hepatology 2019 vol. 7 | 140–148
Wu D.C. et al: Peritoneal tuberculosis: A review
being used, and not all genes being targeted will have the
same sequence.
The gold standard for definitive PTB diagnosis remains
laparoscopy with peritoneal biopsy and subsequent patho-
logical or microbiologic confirmation.57–60 Less invasive
imaging techniques, such as ultrasound and computed
tomography, can also initially be used to detect abdominal
changes common in PTB, such as ascites (free or loculated),
lymphadenopathy, peritoneal thickening and nodules, adhe-
sions, and fibrinous septations.61–63 Additionally, computed
tomography can be combined with 18F-fluorodeoxyglucose
positron emission tomography to increase sensitivity in deter-
mining peritoneal thickening of unknown origin.64 Either com-
puted tomography or ultrasound can be used to facilitate
peritoneal needle biopsy or aspiration of ascitic fluid.65 Our
recommended stepwise approach for the diagnosis of PTB is
detailed in Fig. 3.
Wu D.C. et al: Peritoneal tuberculosis: A review

Table 2. PTB medical treatment in those with liver disease

Concomitant
immunocompromising
conditions Initial therapy Continuation therapy Comments
65
No liver disease 2 months of INH, RIF, PZA and EMB INH and RIF daily for
given dailyu at least an additional 4
months
No liver disease, 2 months of INH, RIF, PZA and EMB INH and RIF daily for As HIV patients are often on many
HIV+ on given daily at least an additional 4 additional medications, caution
antiretroviral months must be used when managing
therapy65 possible drug-drug interactions
between HAART and TB therapy
No liver disease, 2 months of INH, RIF, PZA and EMB INH and RIF daily for
HIV+ not on given daily at least an additional 7
antiretroviral months
therapy/ delayed
response to
therapy67
Treatment failure70 Revision of therapy with at least
three unused medications with at a
minimum one injectable agent
while awaiting sensitivities
Liver disease RIF, PZA and EMB for 6 months
present 12
INH, RIF, EMB for 2 months followed by INH and
RIF for another
7 months
RIF, EMB, a fluoroquinolone,
cycloserine/ injectable agents for
12–18 months
SM, EMB, fluoroquinolone (e.g., Second-line agents:
moxifloxacin), and another second- fluoroquinolones, rifabutin,
line oral drug ethionamide, amino salicylic acid,
cycloserine
u
While additional TB therapies have been found to be equally efficacious in cases of pulmonary disease, listed treatment regimens reflect those that have been trialed
specifically in cases of abdominal tuberculosis.
Abbreviations: EMB, ethambutol; HAART, highly-active antiretroviral therapy; INH, isoniazid; PZA, pyrazinamide; RIF, rifampin; TB, tuberculosis.

Treatment drug regimen, barring any drug-drug interactions with the

Treatment for PTB is pharmacologic, with the drug regimen
consistent with that used for pulmonary TB. Currently, the
five common first-line medications are isoniazid (INH), RIF,
pyrazinamide, ethambutol, and streptomycin. Treatment
duration consists of a four-drug regimen administered for 2
months, with continuation of treatment with RIF and INH for 4
or more months12 (Table 2). Studies examining the efficacy of
prolonged dual-agent continuation therapy for 6 months or
greater have not shown increased efficacy compared to the
standard 4-month regimen.66,67 Response to therapy in PTB
is usually noted within the first 3 months of treatment and is
guided by the resolution of presenting symptoms, such as
ascites and normalization of laboratory values.12 Surgical
intervention in PTB is reserved for cases exhibiting signs of
bowel perforation, intestinal obstruction, fistulae, abscesses,
and hemorrhage.15
For HIV-positive patients on antiretroviral therapy, the TB
treatment regimen does not differ from the aforementioned
antiretroviral medications. For HIV-positive patients not on
antiretroviral therapy at the time of PTB diagnosis or for those
with a delayed response to therapy, it is recommended that
the continuation phase of treatment be extended to 7
months.68
Hepatotoxicity (11% of cases) is the most common cause
of TB therapy discontinuation among all infected patients
treated with combinations of INH, RIF, and pyrazinamide.69 In
those that do not have serious hepatic complications from TB
treatment, asymptomatic elevations in liver enzymes, specif-
ically aspartate aminotransferase (AST), may occur. Unless
enzyme elevations increase to 5 times the normal limit or 3
times the normal limit in the setting of symptomatic liver dys-
function, the treatment should not be altered.12 However, if
there is an increase in liver enzyme levels, the intervals
between scheduled liver function testing should be short-
ened. Other markers of adverse effects of TB therapy
include rising bilirubin and alkaline phosphatase levels.
These should be closely monitored and further investigated

Journal of Clinical and Translational Hepatology 2019 vol. 7 | 140–148 145


for complicating causes, such as worsening TB dissemination
and/or direct infection of the liver/gallbladder. If laboratory
markers or symptoms are severe enough to warrant the tem-
porary cessation of therapy, treatment should not be reiniti-
ated until AST levels are below 2 times the normal threshold.
Once the decision is made to restart therapy, RIF may be
restarted followed by INH, pyrazinamide, and ethambutol at
a week apart.12
Patients with baseline liver disease face potentially serious
complications from PTB treatment. One study showed hep-
atotoxicity rates of 26% in a cohort with baseline liver disease
treated with the standard quadruple-agent therapy with dual-
agent continuation therapy, while another cohort also with
baseline liver disease and treated with INH, RIF, ethambutol
and ofloxacin for 2 months followed by INH and RIF for 10
months, showed no hepatotoxicity.64 Importantly, both
groups achieved 100% response to their respective thera-
pies. While several alternative regimens have been proposed
for patients with liver disease, there is no universally adopted
treatment strategy at this time.70 Unfortunately, delay or
failure to treat TB carries high mortality rates, with one
study showing an overall mortality rate of 35% and a mortal-
ity rate in cirrhotics as high as 73%.71
Corticosteroids have been used in some studies as an
adjuvant therapy during the treatment process of PTB, dating
as far back as the 1960’s.72 The theory behind the use of
corticosteroids revolves around the idea that they reduce
the amount of peritoneal inflammation and fibrosis caused
by the infection and ultimately prevent adhesions that can
lead to intestinal obstruction.73 While some modest benefit
has been noted in small-scale studies, corticosteroids have
not been extensively studied in this capacity and their use in
PTB is not regularly recommended.
Conclusions
PTB is a growing problem due to the rising rates of immune
compromise among the global population. Unfortunately, the
diagnosis of PTB is difficult to make given its nonspecific
symptoms and presentation. While imaging may be helpful in
some presenting cases, paracentesis with fluid analysis
remains paramount for diagnostic work-up. Although newer
molecular biologic diagnostic techniques, such as PCR or
ligase chain reaction, have shown significant promise, at
present they are limited by their high false positive rates.
Ultimately, there is no single laboratory test that can be used
to consistently confirm the diagnosis of PTB, and at this time
invasive studies, such as laparoscopy with peritoneal biopsy
and subsequent histological or microbiologic confirmation,
remain the gold standard for diagnosis.
Treatment of PTB depends on the severity of the disease,
condition of the adaptive immune system, and baseline liver
function. The antibiotic regimen for cases of uncomplicated
PTB does not differ significantly from that of pulmonary TB. In
cases of complicated PTB, such as in patients with HIV, an
extended duration of therapy of at least 7 months is indicated.
Due to the hepatoxicity of the agents used to treat PTB, liver
function should be monitored throughout the course of anti-
biotic use, with treatment cessation only indicated in patients
without signs of liver dysfunction who experience liver
enzyme elevations 5 times the normal limit or in those with
signs of liver dysfunction and elevated liver enzymes 3 times
the normal limit.
146 Journal of Clinical and Translational Hepatology 2019 vol. 7 | 140–148
Wu D.C. et al: Peritoneal tuberculosis: A review
Conflict of interest
The authors have no conflict of interests related to this
publication.
Author contributions
Wrote the manuscript (DCW, LDA), and developed the idea for
the article and critically revised it (GYW).
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